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口腔里面菌群与阿尔茨海默症的原因

李语晨 刘媛 陈峰 初明 陈霄迟

李语晨, 刘媛, 陈峰, 等. 口腔菌群与阿尔茨海默症的关系[J]. koko体育app 学报(医学版), 2022, 53(2): 194-200. doi: 10.12182/20220360304
引用本文: 李语晨, 刘媛, 陈峰, 等. 口腔菌群与阿尔茨海默症的关系[J]. koko体育app 学报(医学版), 2022, 53(2): 194-200. doi:
LI Yu-chen, LIU Yuan, CHEN Feng, et al. Relationship between Oral Microbiota and Alzheimer's Disease[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCE EDITION), 2022, 53(2): 194-200. doi: 10.12182/20220360304
Citation: LI Yu-chen, LIU Yuan, CHEN Feng, et al. Relationship between Oral Microbiota and Alzheimer's Disease[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCE EDITION), 2022, 53(2): 194-200. doi:

口腔菌群与阿尔茨海默症的关系

doi: 
基金项目: 国家自然科学基金(No. 81991501)、口腔疾病研究国家重点实验室开放课题基金(No. SKLOD2021OF03)和北京大学医学部与英国伦敦国王大学联合基金(No. BMU2020KCL003)资助
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    E-mail:chenfeng2011@hsc.pku.edu.cn

Relationship between Oral Microbiota and Alzheimer's Disease

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  • 摘要: 阿尔茨海默症(Alzheimer’s disease, AD)是一种常见的神经退行性疾病。在老龄化社会中,AD的高患病率和低生活质量给个人、家庭和社会带来严重困扰,但AD的病因和致病机制并未完全明确,年龄、遗传、环境等因素都与之有关,治疗也没有令人满意的效果。最近有研究表示,口腔菌群失调与AD发病有密切关系,口腔细菌感染可能是引发AD的病因之一。口腔是人体最大的微生物生态系统,其稳态对健康至关重要。口腔菌群紊乱导致的细菌感染会通过直接和间接作用造成大脑内β-淀粉样蛋白(amyloid β-protein, Aβ)代谢失衡,Tau蛋白过磷酸化,沉积形成老年斑和神经原纤维缠结(neurofibrillary tangles, NFTs)损伤神经元。本文根据最新的研究进展,讨论口腔菌群与AD发生的相关性和机制,以及主要口腔细菌的致病机制,探索口腔菌群靶向疗法的潜在应用前景。
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    图  1  口腔菌群对脑组织的直接损伤作用

    Figure  1.  ᩚᩚᩚᩚᩚᩚ⁤⁤⁤⁤ᩚ⁤⁤⁤⁤ᩚ⁤⁤⁤⁤ᩚ𒀱ᩚᩚᩚ Direct damage of oral microflora to brain tissue

    A: Some bacteria can directly produce Aβ precipitation accumulation in brain tissue; B: Microglia are continuously activated by bacteria and toxins entering brain tissue, releasing inflammatory factors and causing neuroinflammation; C: Bacteria and toxins activate the complement system; D: Inflammatory factors and complement fragments promote Aβ precipitation and Tau protein hyperphosphorylation; E: Aβ precipitation and hyperphosphorylation of Tau protein stimulate microglia to produce inflammatory factors that maintain or exacerbate neuroinflammation; F: Excessive Aβ precipitation and hyperphosphorylated Tau protein damage neurons and induce AD. OMV: Outer membrane vesicle; LPS: Lipopolysaccharide; TNF: Tumor necrosis factor; Aβ: Amyloid β-protein; IL-1: Interleukin-1; IL-6: Interleukin-6; IL-12: Interleukin-12; IL-23: Interleukin-23.

    图  2  细菌、毒素和炎症因子通过BBB途径

    Figure  2.  🍌 Bacteria, toxins and inflammatory factors pass through the BBB pathway

    A: Destruction of BBB barrier cells; B: Activating barrier cells to secret nitric oxide (NO), prostaglandin (PG) and other signaling molecules, and promoting brain cells to produce inflammatory factors, such as LPS-stimulated IL-6; C: Cell-specific transporters transporting inflammatory factors, such as TNF transporters. OMV: Outer membrane vesicle; LPS: Lipopolysaccharide; TNF: Tumor necrosis factor; IL-1: Interleukin-1; IL-6: Interleukin-6; BBB: Blood-brain barrier.
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出版历程
  • 收稿日期:  2022-10-17
  • 录用日期:  2023-02-21
  • 修回日期:  2023-02-19
  • 刊出日期:  2023-03-22

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